What is it about?
Hepatocellular carcinoma (HCC) is a highly aggressive and leading cause of cancer-related deaths worldwide. One of the key mechanisms involved inside these cancer cells is a specific signaling pathway called the PI3K/AKT/mTOR (PAM) pathway regulating cell growth, survival, metabolism, and multiplication. When this pathway becomes overactive, it causes cells to multiply rapidly, and spread to other parts of the body. Since available treatments face challenges like drug resistance, scientists are looking at natural alternatives such as flavonoids. They can successfully block the hyperactive PAM pathway in following ways: -Starving the cancer: They directly stop the signals that tell cancer cells to grow and divide. -Boosting chemotherapy: They make cancer cells more sensitive to traditional treatments, reducing the chances that the cancer will become resistant to drugs. -Managing cellular stress: They act as antioxidants, altering the internal environment of the cancer cell to force it to self-destruct. However, further research is required before they hit the market for patients. Researchers must focus on pharmacokinetics—understanding how the human body absorbs, break downs, and transport these compounds to the liver.
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Why is it important?
This paper targets the research done on specific pathway involved in liver cancer and this review shows a path between natural substances and their mechanism. It also points out the missing part- pharmacokinetics of these molecules.
Perspectives
Half of all liver cancer patients have a hyperactive cellular pathway that causes rapid tumor growth and resists traditional chemotherapy. I hope this review shows how flavonoids can safely block this cellular pathway and open the door for more effective and low toxicity combination treatments.
Asma Naqi
Jamia Hamdard
Read the Original
This page is a summary of: Regulation of the PI3K/AKT/mTOR cascade in Hepatocellular Carcinoma Using Flavonoid Molecules, Current Cancer Drug Targets, October 2025, Bentham Science Publishers,
DOI: 10.2174/0115680096389157250917055438.
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